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Selected AbstractsEnhanced glycogenesis is involved in cellular senescence via GSK3/GS modulationAGING CELL, Issue 6 2008Yong-Hak Seo Summary Glycogen biogenesis and its response to physiological stimuli have often been implicated in age-related diseases. However, their direct relationships to cell senescence and aging have not been clearly elucidated. Here, we report the central involvement of enhanced glycogenesis in cellular senescence. Glycogen accumulation, glycogen synthase (GS) activation, and glycogen synthase kinase 3 (GSK3) inactivation commonly occurred in diverse cellular senescence models, including the liver tissues of aging F344 rats. Subcytotoxic concentrations of GSK3 inhibitors (SB415286 and LiCl) were sufficient to induce cellular senescence with increased glycogenesis. Interestingly, the SB415286-induced glycogenesis was irreversible, as were increased levels of reactive oxygen species and gain of senescence phenotypes. Blocking GSK3 activity using siRNA or dominant negative mutant (GSK3,-K85A) also effectively induced senescence phenotypes, and GS knock-down significantly attenuated the stress-induced senescence phenotypes. Taken together, these results clearly demonstrate that augmented glycogenesis is not only common, but is also directly linked to cellular senescence and aging, suggesting GSK3 and GS as novel modulators of senescence, and providing new insight into the metabolic backgrounds of aging and aging-related pathogenesis. [source] Restoration of Lake Geneva: Expected versus observed responses of phytoplankton to decreases in phosphorusLAKES & RESERVOIRS: RESEARCH AND MANAGEMENT, Issue 2 2002Orlane Anneville Abstract Long-term phytoplankton responses in Lake Geneva to a decline in phosphorus (P) loading are examined in terms of summer (July,September) biomass and community structure. With the rapid development of human activity on its banks and within its catchment area in the 1960s, this large subalpine hydrosystem shifted from oligotrophy to eutrophy within approximately one decade. Measures to reduce P loading were initiated successfully in the mid-1970s, when total P concentrations in the winter overturn altered from 90 ,g/L in 1980 to 40 ,g/L in 1998. Until the 1990s, algal descriptors improved as expected (biomass decline, reappearance of diatom species, increased contribution of nanoplankton). Then, paradoxically, and in contrast to the reappearance of oligotrophic species, summer algal biomass began to increase. Pre-summer (period prior to the beginning of the clear water phase) dissolved inorganic phosphorus concentrations and summer phytoplankton composition presented similar interannual trends. However, the succession of phytoplankton structure during the reoligotrophication phase differed greatly from that during the eutrophication period, and a recent abnormal upward trend in algal densities is mainly the result of the development of large species that formerly were only common from late September until November. This community change, mainly triggered by filamentous (Mougeotia gracillima, Tribonema) or motile forms (Dinobryon sociale, Cryptophycea), seems to have been induced by the earlier and greater deepening of the P-depleted layer. In addition to milder summers, this massive development of larger forms seems to be favoured by four of their biological features: tolerance to warm temperatures, tolerance to low-light intensity (might exploit deeper layers where P is not yet limiting), shapes not only providing a large surface to volume ratio or motility (adaptation to low-nutrient concentrations), but increasing resistance to zooplankton grazing. This paradoxical trend, perhaps reinforced by the decline on roach Rutilus rutilus abundance (an opportunistic planktivore), is likely to remain until the P-depleted zone is extended below the layers that can be frequently resupplied in nutrients by hydrodynamic processes. [source] Recent trends in diagnosis and treatment of faecal incontinenceALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2004A. K. Tuteja Summary The inability to control bowel discharge is not only common but extremely distressing. It has a negative impact on a patient's lifestyle, leads to a loss of self-esteem, social isolation and a diminished quality of life. Faecal incontinence is often due to multiple pathogenic mechanisms and rarely due to a single factor. Normal continence to stool is maintained by the structural and functional integrity of the anorectal unit. Consequently, disruption of the normal anatomy or physiology of the anorectal unit leads to faecal incontinence. Currently, several diagnostic tests are available that can provide an insight regarding the pathophysiology of faecal incontinence and thereby guide management. The treatment of faecal incontinence includes medical, surgical or behavioural approaches. Today, by using logical approach to management, it is possible to improve symptoms and bowel function in many of these patients. [source] Li,Fraumeni and Li,Fraumeni-like syndrome mutations in p53 are associated with exonic methylation and splicing regulatory elementsMOLECULAR CARCINOGENESIS, Issue 10 2009Sofia Kouidou Abstract Mutations in codon 133 of p53, which cause the loss of the ,133 isoform(s) expression, are very frequent in the Li,Fraumeni (LF) and Li,Fraumeni-like (LFL) syndromes. In sporadic cancers, silent p53 mutations are correlated with exonic splicing enhancers (ESEs) and exonic methylated sites. The present study shows that mutations in splice sites are also very frequent in LF/LFL syndromes, while missense mutations are less common compared to other familial or sporadic cancers (P,=,0 in both cases). Furthermore, it is shown that the codons at which LF/LFL germline missense mutations occur, correlate with CpG-containing ESEs (r,=,0.181, P,=,0.014) which are all methylated in p53. While both silent and LF/LFL missense mutations correlate with SC35 motifs, only the latter are associated with SRp55. On the contrary, only silent mutations in sporadic cancers correlate with SF2/ASF motifs in p53. Moreover, 12.1% of LF/LFL missense mutations involve the formation of potential splice sites of considerable splicing scores. Finally, mutations that are not at, or adjacent to CpGs (±1 codon, 34% of all LF/LFL mutated sites), introduce considerable changes of the ESE scores (>1.3 score change). The above data verify that LF/LFL missense mutations probably result also in splicing deregulation, in addition to any changes of the protein function and are mostly associated with alterations of the exonic methylation landscape. Some of the ESEs affected in LF/LFL syndromes are also genetically unstable in sporadic cancers but non-CpG cytosine instability, which is predominantly associated with specific ESEs, is only common in sporadic cancers. Mol. Carcinog. © 2009 Wiley-Liss, Inc. [source] Prevalence of chronic bronchitis and chronic respiratory symptoms in adults over the age of 35 years in Isfahan, Iran in 1998RESPIROLOGY, Issue 3 2001Mohammad Golshan Objective: Chronic obstructive airways disease (COPD) in older patients is reported to be not only common, but also frequently overlooked and untreated by general practitioners. Chronic bronchitis is one of the major components of COPD and can be readily screened. This study investigates the prevalence of chronic bronchitis and related symptoms in Iran with special reference to COPD. Methodology: A random sample of 4636 participants aged 35 years and over, attended a research clinic for interview and physical examinations. Those reporting classic symptoms of chronic bronchitis were referred to a pulmonary clinic for pulmonary function testing. Results: Two hundred and sixteen patients (4.65%) had chronic bronchitis. Among these, 78 (36.1%) had obstructive airways disease. Decreased forced expiratory volume in 1 s/forced vital capacity to levels of less than 70% were recorded in 45 patients (42.9% of the tested population). Less than 25% of the patients had a previous diagnosis of chronic bronchitis and/or airways disease. Conclusion: Obstructive airway diseases are under-diagnosed in developing countries. Physicians practising in such areas of the world should be aware, and try to detect the subclinical illnesses, especially in urban areas. [source] Detection of Rare Nonsynonymous Variants in TGFB1 in Otosclerosis PatientsANNALS OF HUMAN GENETICS, Issue 2 2009M. Thys Summary Otosclerosis is one of the most common forms of hearing loss in the European population. We have identified a SNP in the TGFB1 (transforming growth factor beta 1) gene that is associated with susceptibility to otosclerosis. The protective allele of this variant, with isoleucine at position 263 of the protein, is more biologically active than the risk allele, which has a threonine in this position. Because recent studies have shown that not only common, but also rare variants can be involved in complex diseases, we performed DNA sequence analysis of the exons and intron-exon boundaries of TGFB1 in 755 otosclerosis patients and 877 control samples. We found 3 different nonsynonymous variants (E29, A29 and I241) in four otosclerosis patients, but no such changes were found in controls. In silico analysis shows that these variations could influence TGF-,1 function and activity. Taking into account that most rare missense alleles are thought to have a biological effect, the data suggest that multiple rare amino acid changing variants in TGF-,1 may contribute to susceptibility to otosclerosis. [source] | |||||||||||||